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- Title
Involvement of reactive oxygen species and high-voltage-activated calcium currents in nanoparticle zinc oxide-induced cytotoxicity in vitro.
- Authors
Zhao, Jingxia; Yao, Yang; Liu, Shichang; Zhang, Tao; Ren, Guogang; Yang, Zhuo
- Abstract
This study was to determine the possible neurotoxicity and mechanisms underlying the effects of nano-ZnO with sizes of 20-80 nm on central nervous system (CNS). The cytotoxicity of nano-ZnO was investigated in PC12 cells. The viability of cells was observed by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and the generation of reactive oxygen species (ROS) for cells was evaluated by a fluorometry assay. The apoptosis of cells was detected and analyzed by flow cytometry. In addition, effects of nano-ZnO on the properties of high-voltage-activated (HVA) calcium currents were studied in acutely isolated rat hippocampal pyramidal neurons using the whole-cell patch clamp technique. The results of MTT assay showed that nano-ZnO (10 g/mL) caused a significant decrease in cell viability ( P < 0.05). Nano-ZnO induced intracellular accumulation of ROS and the apoptosis of PC12 cells with the increasing concentration of nano-ZnO in flow cytometric assay ( P < 0.05). Further results of electrophysiological recording indicated that 10 g/mL nano-ZnO first altered the current-voltage curve and the peak amplitudes of HVA calcium currents at 10 min of the recording, and the peak current amplitudes were increased significantly at the end of 30 min ( P < 0.05). All these results suggested that the increase of intracellular ROS was one of potential mechanisms of cellular apoptosis induced by nano-ZnO. Nano-ZnO could cause the elevation of cytosolic calcium levels by enhancement of HVA calcium currents, which would increase the generation of intracellular ROS, and consequently promote the neuronal apoptosis.
- Subjects
NEUROTOXICOLOGY; CENTRAL nervous system; REACTIVE oxygen species; APOPTOSIS; ZINC oxide; CALCIUM
- Publication
Journal of Nanoparticle Research, 2012, Vol 14, Issue 11, p1
- ISSN
1388-0764
- Publication type
Article
- DOI
10.1007/s11051-012-1238-1